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Type 1 diabetes (T1D) results from autoimmune destruction of pancreatic β-cells. While anti-CD3 therapy can delay disease progression and preserve residual β-cell function, disease reversal will likely require both immune modulation and β-cell regeneration. We found that the combination of harmine and exendin-4 (H+E) r...
Exposure of T1D-associated cytokines to primary human ductal cells altered cargo of secreted EVs, suggesting a previously unknown ductal cell communication pathway with a potential implication for modulating beta cells during T1D progression.
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